For many years mitochondria have been implicated in the process of carcinogenesis. At the beginning of 20th century Otto Warburg has started research focused on failure of oxadative metabolism in cancer cells. In his work he described disruption of respiration as typical for cancer cells. Warburgs discovery resulted in establishment of many projects focused on the role of mitochondria in cell transformation. Since that time multiple reasearch groups have reported mitochondria DNA mutations in majority types of cancer.

Supernumerary, old or damaged cells of multicellular organisms are eliminated by apoptosis – programmed cell death. Apoptosis is accompanied by series of characteristic morphological and biochemi- cal events. The cell activates a cascade of cysteine proteases – caspases, that digest target proteins. Nucleases are also activated, which together leads to irreversible cell damage within few hours. Mitochon- dria are the cell compartment that integrates signals from different apoptotic pathways activated by ischemia, heat shock or growth hormones depletion.

For several decades, it has been assumed that plasminogen activation may play an important role in tumor invasion and metastasis. The basic idea is that plasminogen activators released from cancer cells catalyze the proteolytic conversion of the inactive zymogen plasminogen to the active proteinase plasmin, which in turn catalyzes degradation of proteins in basement membranes and extracellular matrix (ECM) and thus facilitates cancer cell invasion into the surrounding tissue.

Cell death, commonly recognized as necrosis or apoptosis, is thought to be a one of biological processes describing cell life. The phenomena of cell recycling during human life is known for a various types of cells and the resistance of cancer cells to apoptosis is also well described. Proapoptotic gene therapy is one of the method of cancer therapy. The main rationales are focused on induction of apopto- sis of cancer cells and therefore inhibition its growth. Mostly, gene therapy trials are concerned on genes encoding well known proteins of apoptotic signaling as BAX, P53, TNF, caspases.

The early diagnosis, treatment and prevention of cancer recurrence are the major priorities in future oncology. An increasing number of cases are surgically cured as a result of early diagnosis and novel approaches to chemo and radiotherapy. However, a significant percentage of these patients will develop recurrent and/or metastatic disease. The prognosis for patients with metastatic breast, lung and colorectal cancers at diagnosis or as a cancer recurrence are poor.

The cell cycle is regulated by the activity of cyclin dependent kinases (CDKs) associated with cyclins. Their activity is opposed by various CDK inhibitory proteins. Disregulation of the cell cycle occurs in various pathological conditions - the most important of them being cancer. Therefore, there is a continuous effort to search for chemical CDK inhibitors, which may be used as antiproliferative drugs. Various compounds have been already isolated and synthesized (e.g. olomoucin, roscovitine, flavopiridol and indirrubin). All known CDK inhibitors compete with ATP in the binding with CDKs.

In aging population growing up rapidly causes of cancers are observed. Lost of immunological answer caused by DNA double-strand breakes, longer exposition to carcinogens, decreasing activity of DNA-repair system in aging cells, defects of supressor genes are caused carcinogenesis. DNA-defects of aging and cancer cells by hipermethylation GpC island of gene promoters are observed. Changes in extracellular matrix of aging and transformed cells are responsible forcell migration causing metastasis.

In the article a short description is given of genes involved in the development of neoplasia including tumour suppressors and oncogenes as well as the minimal number of changes required to transform a normal cell into a neoplastic one. Changes detected in mitochondrial DNA in solid tumours are also mentioned.

The trefoil family of peptides is mainly associated with gastrointestinal tract. These peptides protect the mucous layer. The protective role of trefoil peptides is explained by their interaction with carbohydrates attached to mucin glycoproteins and by maintenance of the mucus structure. Trefoil peptides influence migration of epithelial cells and thus contribute to regeneration of the mucous layer. A correlation between trefoil peptides and oncogenesis remains unclear.